Monty and Gonzalo,

From your own personal experience, have you found/noticed significant improvement of your CH when consuming tryptophan rich food ?

If you have, is there a particular combination/list of food that you found to be reliably effective ? What is the time frame you recommend  for such diet change ?

Thanks for sharing.

Note also, while there are many people that believe that 5-htp helps migraine (and articles to support this), the consensus seems to be that SSRIs don't do much for migraine.  Whether or not this transfers over to clusters, I don't know. But it does lend some support to previous ideas that SSRIs are somewhat different than raising serotonin everywhere.

Summary of Assumptions

This scheme will serve as a benchmark for the discussion and must be completed as various items contained are discussed.

Bases of the hypothesis

   1) The trigeminal nerve is extremely sensitive in patients with CH and ignites more easily from the normal.
   2) The levels of serotonin are crucial for controlling the cycles of crisis and the need for action on its specific receptors responsible for vasoconstriction in the cranial vessels.

Actions based on theoretical assumptions

1) Prevent or reduce inflammation

    A) To improve the overall fitness of the nerve
    B) Avoid physical damage to the nerve
    C) To avoid an excessive and continuous expansion of the cranial vessels
    D) To promote the constriction of cranial vessels

2) Increasing the production of serotonin

    A) Increase the availability of the precursor tryptophan
    B) Reduce the metabolism of tryptophan to different pathways than the serotonin pathway.
    C) Improving the production of serotonin improving it pathway of tryptophan metabolites

3) To reduce losses or decreases in serotonin

    A) Outstanding (MAOI ?...)

4) Avoid storage of serotonin increasing free serotonin

    A) Outstanding (SSRI's ....)

5) Improve the effectiveness of serotonin available

    A) Outstanding (receivers ...)

Kevin_M wrote on Feb 24^th, 2009 at 6:29am:



Gonzalo, I agree with Kevin.

My biggest problem with your hypothesis is that if what you said above is true, then all CHers should have symptoms of trigeminal neuralgia, but we dont.

One of the most striking feature of trigeminal neuralgia is the severe pain caused by chewing, while in CH the pain is only present and severe during a hit. Outside a hit, a CHer can chew without feeling pain.

It doesnt seem that in CHers, the trigeminal nerve is extremely sensitive nor damaged.

Quote:


CH has been classified as a type of trigeminal neuralgia - intermittent, to be sure, of a different frequency than classic trigeminal neuralgia, but a case where there is undoubtedly trigeminal nerve pain.

The trigeminal is getting inputs from the brain,and from peripheral areas. It processes those inputs, and then fires when the threshold is reached.

I think that was distinguishes CH from classical TN is that the hypothalamus is the strongest driver in clusters, while peripheral is more important in classic TN. In classic TN, triggers include brushing the hair, touching the face, yawning.

But peripheral input could be a factor in CH- allergies, rhinovirus infections, TMJ jaw issues, neuromuscular lesions, etc are all suspect in some people.

The trigeminal could be damaged and still function adequately under normal circumstances. It only becomes obviously dysfunctional when 'stress' hits a certain level.

monty wrote on Feb 24^th, 2009 at 2:55pm:



You are missing the point here Flo. I am not saying that CH does not have trigeminal neuralgic pain. What I am saying is that CH does not have symptoms of a damaged trigeminal nerve. It is the hypothalamus that is malfunctioning not the trigeminal nerve.

Gonzalo's hypothesis "requires" the trigeminal nerve to be damaged and therefore extra sensitive to any and all signals.

I am saying that in CH the trigeminal does not have to be damaged at all but can still fire abnormal signals because its control centre is off.

Gonzalo's hypothesis focusses on the trigeminal nerve as the centre of action in CH and he speculates that by " supporting " a damaged and oversensitive TN with various varying factors will help CH.

I on the other hand says that the TN is only a small player in the picture of CH. It is the pineal gland and the hypothalamus we should focus on. If those 2 glands are malfunctioning, then no matter how much we "nurture" the TN its going to fire abnormally in a hit.

Quote:


That is a common perspective and there are many researchers focused on the hypothalamus.  I don't deny the importance of the hypothalamus, but think that the trigeminal itself is important. Reasons include:

1) Non-Hypothalamic cluster headache documented by Rozen.
2) Phantom clusters - all the autonomic symptoms, no pain from trigeminal.
3) Research that suggests that problems with trigeminal may be common in CH, and that improvement is seen if possible to treat trigeminal lesions.
4) Nerve blocks - they don't involve injections to the hypothalamus.
5) Myofascial therapy can be an effective treatment.
6) Association of clusters with sinus issues, TMJ jaw problems.
7) Immunology - trigeminal nerve more likely to be affected than hypothalamus by epstein-barr virus or other viruses that are more common in CH.

1) Rozen's work on this is preliminary, but worth considering, even if it is a minority of cases.

2) I have experienced phantom clusters, and I believe it is the hypothalamus going haywire, but the trigeminal does not respond by releasing pain inducing substances. If this is true, then it offers treatment options for the pain - not a complete therapy, but less excruciating agony.

3) See Multimedia File Viewing and Clickable Links are available for Registered Members only!!  You need to or

4) Nerve blocks reduce peripheral inputs to other areas; the most effective is a sphenopalatine, which is part of the trigeminal nerve.

5) Myofascial therapy - recently show to help with CH. A reduction of peripheral inputs to trigeminal from muscles in head makes the most sense, the hypothalamus is not directly affected by such procedures, but the trigeminal is.

6) A ten year follow-up study on endonasal surgery for clusters found about 1/3 of patients who got surgery went into remission and were there for ten years, about 1/3 displayed marked improvement. The hypothalamus-centered theory cannot explain this. Not everyone with clusters has such contact points, but those who do seem to benefit benefit from treating them. Other related problems include chronic sinusitis, tmj ... my impression is that they are more common in CH, although there is not a lot of data on that.

So I am not trying to erase the role of the pineal and hypothalamus - they are important and clearly contribute. That is a very good explanation of the timing that many of us have for headaches. The hypothalamus is a source of input to the trigeminal that can make it scream.  But I think the immediate source of the pain is the trigeminal behind the eye, and this is important. Sometimes the trigeminal can scream bloody cluster even when the hypothalamus is quiet, and sometimes the hypothalamus is hitting the trigeminal full blast, but the trigeminal does not scream.

Hey, Monty

Indeed, the 2A is only diet, and focused only on the availability of tryptophan, because the diet should be reviewed to other substances that may be beneficial or harmful in other ways.

you entered 2B, I was somewhat prepared 2C, so I let it posted and so we can discuss both at a time; most of the documents we'll read cover two questions together.

2B respect, you let me really surprised, does not have the slightest idea of what's what, but I'll learn. But two important things: first, is that not only is the IDO, also the 2.3-tryptophan dioxygenase (t-pyrrolase), hereinafter TDO, and not just to do the substances that block them ("good"), but those who powers them, too ("bad"). So we have four areas of work with the inhibitors/enhancers of IDO/TDO.

One final point about it: I believe that the path of the bacterial metabolism of tryptophan in the intestine did not affect us, in fact we know that 90% of serotonin is in it. I think we must focus in only the L-Tryptophan absorbed from the intestine to the bloodstream. You'll say.

Because these days I work a lot, I present 2C issue without too much depth, and I hope we will gradually deepen it. And here is:

---

In principle, as I said, the process is:

1) Tryptofhan + enzyme T-tryptophan hydroxylase (TPOH) + cofactor tetrahidrobiopterín => 5-Hydroxytryptophan (5HTP).

2) 5HTP + 5-Hydroxytryptophan decarboxylase + cofactor priridoxal phosphate => serotonin (5HT).

These are the direct factors, but there are many other indirect essential for any cause for the process. They are:

- Vitamin B2 (riboflavin)
- Iron
- Magnesium
- Vitamin C (ascorbic acid)
- Oxygen

I think the tetrahidrobiopterin deficit should not be considered, because its lack causes serious diseases, so it should be guaranteed levels. The rest of actors are:

TPOH.- In the process (1) tryptophan=> 5HTP acts as, and emphasize this many authors, limiting factor. It is in the air how to improve their standards or to prevent their relegation.
5-HTP decarboxylase. - No idea.
Vitamin B6 .- Essential to have pyridoxal phosphate.
Vitamin B2.- Essential to transform B6, pyridoxine phosphate, into pyridoxal phosphate.
Iron, magnesium.- It is said in many reviews, but I have not come to see the mechanism by which they operate.
Vitamin C.- It's said in many reviews, too, but I have not found the mechanism by which they operate. At least it is necessary to get the iron.
Oxygen.- Essential for the oxidation process (1). As I said, I believe that its importance extends to other important issues, as we'll see.

And it rest the possibilty of intake 5-HTP directly ...........

---

And I say something I thought while I was studying this about the 5-HTP intake: it's possible that people whose process (1) is reduced can see CH improved by the 5-HTP intake because finally they have it.
But other people with problems at process (2) due for example, in the absence of B2 and/or B6, were found with excessive levels of 5-HTP, their own plus the intaked, and since 5-HTP is a competitor of serotonin (like melatonin itself and other similar substances) by the same receptors, this would explain that they feel bad, they should have something similar to the symptoms of the hypersertoninérgic syndrome ... it would be nice to check the symptoms of those who have felt bad with 5-HTP.

Finally, if you, Monty (there's someone more ...?) could copy/paste and polish the 2A resume (of course you now I do my best, but that's not enough), I would like to insert it in the "resume". This way, with a link inserted in the first post to it, everybody could easily read latest "conclusions". Do you think it's a good idea?

Best regards

wagwoman wrote on Feb 28^th, 2009 at 7:24pm:

Hello,

I think it's important to put on the table a formal summary of the data medium, substances and processes that affect serotonin before discussing, and I personally will enjoy doing it, about concrete situations. Such discussions might be to force us to delete or add things, or leave all or part undone.

Particularly with respect to the exercise, I have in mind, and I speak of memory, two contradictory data: the first is that physical exertion produces lack of oxygene, hypoxia, and cortisol is generated and this would produce T-pirrolasa so serotonin will decrease. The second is that if you practice a certain exercise intensity for space exceeding 30 minutes, the body activates a whole system of hormonal secretion, including growth (HGH), which completely alters the state after the exercise. But there must be intense and more than 30 minutes, otherwise there is no such download.

So a simple effort could call the beast, but the exercise seriously, it might scare. Who knows, we need to find and compare information and ideas, but we will get this, or I hope so.

Monty

I am searching and reading everything I get of IDO in Spanish, and I'm reading again and again works on the immune system and cancer, especially bowel. I have it already mania, it seems a bad thing, the IDO.

For now, not a single detail of what inhibits or improves its levels, of course you have a prodigious source of information or I am a bit clumsy ... or both. I continue to do so; when I get bored of Spanish will turn to French and I'll comment if I find interesting things.

Regards.

Reading this thread leaves a lot of room for confusion for laymen like myself.

I understand the hypothesis in regards to increase and decrease of serotonin and its pathways. Its a noble effort and appreciated very much.

I think for any of the inputs posted to ultimately make some sense and add inputs from others, there would be a need to back up and attempt to determine what is a normal level of serotonin in humankind if one exists, its usage and variations.
Not sure science itself has moved that far.
Then the discussion of what changes that, could continue and prove more beneficial to a lot of us.

My own observations as well as others may be based more on personal experience and how certain dietary foods can cause those alterations in serotonin usage and pathways.
Those in the know can make some assumptions regarding those inputs, ie: grapefruit and other affecting foods.

The trigeminal nerve and hypothalamus etc.. firings and bypass do appear to be related to serotonin and the previous discourse is indeed beneficial but that need remains to understand why or where normality exists and why modify these inputs whether through dietary or other means.

A lot of benefit can come from random inputs when there are those that can assimilate those inputs into the hypothesis. not easy staying on track.

The larger part of my confusion is related to the why's of increasing serotonin when my experience shows the possible blocking of increased serotonin in certain brain pathways/receptors is beneficial.
I do understand the efforts to explain the fabrication or alteration of serotonin just how its potential benefit exists in our aide has allways escaped me without first finding a benchmark to go by.

An added thought is that these discussions may ultimately help to understand the variations in CH. Why some folks get as little as 1 0r 2 hits a week and some get hit as many as 10 or more times per 24 hrs.

Gonzalo wrote on Mar 1^st, 2009 at 6:52pm:


I am saying we don't know for sure.  In a healthy person, if we deprive them of tryptophan, that will lower serotonin and lower melatonin.  If we then return that person to a healthy diet, serotonin goes up and then melatonin goes up. In that scenario, it is straightforward.

In cluster headaches, it may just as simple, or there may be something more.  We don't know why the melatonin curve for people with cluster headaches is flatter or completely flat, when normal people have a nice peak that corresponds to night and a valley that corresponds to day.  There could be many reasons for this - one is a lack of serotonin, the necessary building block.  But it could be something else - maybe in some people, there is enough serotonin, but there is something else lacking.  Maybe the pineal isn't working properly, maybe there is an endocrine issue (gonadotropin and corticotropin problem).

When I took 5-htp, I felt that I slept much better, so in my case I believe that increasing serotonin did increase melatonin.